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논문 기본 정보

자료유형
학술저널
저자정보
Hosseini Marjan (Department of Physiology School of Medicine Tehran University of Medical Sciences) Parviz Mohsen (Department of Physiology School of Medicine Tehran University of Medical Sciences) Shabanzadeh Alireza P. (Department of Physiology School of Medicine Tehran University of Medical Sciences) Zamani Elham (Department of Physiology School of Medicine Tehran University of Medical Science)
저널정보
대한척추외과학회 Asian Spine Journal Asian Spine Journal Vol.15 No.2
발행연도
2021.1
수록면
200 - 206 (7page)

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Study Design: In this study, we decided to change the activity of periaqueductal gray (PAG)'s metabotropic glutamate receptors subtype 8 (mGluR8) by means of its specific agonist, (S)-3,4-dicarboxyphenylglycine (DCPG), and by knock downing it with mGluR8 siRNA. We then evaluated the changes in animal pain threshold levels in the face of painful thermal stimuli (thermal hyperalgesia).Purpose: Although several mechanisms have been examined for central neuropathic pain, researchers have so far failed to find the precise mechanism for the development and progression of this type of pain. Hyperalgesia is one of the most important complications of central neuropathic pain and there is not a consensus among researchers about the exact cause of this complication. In this study, we investigated the effect of activation of the PAG region mGluR8 on the threshold of pain response to thermal noxious stimulus in rats and measured mGluR8 expression.Overview of Literature: Spinal cord injury (SCI) produces an decrease in mGluR2/3 expression in the injured and vehicle-treated groups compared to normal levels, APDC and L-AP4 treated groups had higher expression levels of mGluR2/3. These findings suggesting that the level of mGluR expression after SCI may modulate nociceptive responses.Methods: Male Wistar rats were randomly assigned to five groups (n=10 per group). The clip compression injury model was used to induce chronic central neuropathic pain. Three weeks after SCI, DCPG, siRNA, or normal saline were administered to the intra-ventrolateral PAG region. Withdrawal threshold to the noxious thermal stimulus (e.g., heat hyperalgesia) was assessed through the tail-flick test. In order to assure involvement of this receptor, pain responses were compared with mice that received GRM8 siRNA.Results: We found that the mGluR8 agonist DCPG increased lead to an increased expression of mGluR8 in the PAG region. We also found that SCI can decrease the threshold of response to painful thermal stimuli; however, activation of mGluR8 with DCPG agonist did not significantly improve the tail-flick response.Conclusions: The results revealed that activation of mGluR8 in PAG is not capable of improving the thermal hyperalgesia threshold. Based on the decreased expression of mGluR8 after SCI induced by clip compression injury and its significant increase after treatment of siRNA against mGluR8, this method might still hold promise as an effective treatment of neuropathic pain. It can be concluded that increased expression of mGluR8 is due to the fact that DCPG prevents the death of neurons that express these receptors.
#Hyperalgesia #Metabotropic glutamate receptor 8 #Spinal cord injuries #3 #4-Dicarboxyphenylglycine #Periaqueductal gray #Neuralgia

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참고문헌 (22)

참고문헌 신청
Merskey HE / 1986 / Classification of chronic pain: descriptions of chronic pain syndromes and definitions of pain terms / Pain (Suppl 3):226 google schola Bonica JJ / 1993 / Evolution and current status of pain programs / J Pharm Care Pain Symptom Control 1:31~44 google schola Devor M / 1983 / Nerve pathophysiology and mechanisms of pain in causalgia / J Auton Nerv Syst 7:371~384 google schola Munglani R / 1995 / Molecular biology of pain / Br J Anaesth 75:186~192 google schola Mohammadzadeh F / 2015 / A fairly comprehensive survey of chronic pain in Iranian population : prevalence, risk factors, and impact on daily life / Health Scope 4:e25467 google schola

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